Senescence
Definition
Senescence is the process by which cells permanently cease dividing while remaining metabolically active. Unlike apoptosis (programmed cell death), senescent cells persist in tissues and accumulate with age, secreting pro-inflammatory molecules that affect surrounding cells and tissue function.
Types and Triggers
Cellular senescence can be triggered by several mechanisms:
- Replicative senescence — Caused by progressive telomere shortening after repeated cell divisions (the Hayflick limit)
- Oncogene-induced senescence (OIS) — A tumour-suppressive response to aberrant oncogene activation
- Stress-induced premature senescence (SIPS) — Triggered by DNA damage, oxidative stress, or mitochondrial dysfunction
- Therapy-induced senescence — Caused by radiation or chemotherapy
The Senescence-Associated Secretory Phenotype (SASP)
Senescent cells secrete a complex mixture of cytokines (IL-6, IL-8), chemokines, proteases (MMPs), and growth factors collectively termed the SASP. While SASP aids wound healing and immune clearance in acute contexts, chronic SASP drives tissue inflammation, fibrosis, and dysfunction — contributing to age-related pathologies.
Relevance to Peptide Research
Senescence intersects with peptide research through several pathways. Epitalon is studied for its effects on telomerase activation, potentially delaying replicative senescence. GHK-Cu has been investigated for modulating gene expression patterns associated with tissue ageing and senescence. Humanin and MOTS-c, as mitochondrial-derived peptides, are studied in the context of mitochondrial dysfunction-driven senescence. The emerging field of senolytics (compounds that selectively clear senescent cells) represents a growing area of interest in longevity research.
Related Peptides
Peptide profiles that reference “Senescence” in their research content.